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By Marissa Boucher and Kimberlee West

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Cerulein-induced pancreatitis was shown to induce senescence of pancreatic ductal cells, in a p16Ink4a (but not p53) dependent manner, 8 and quite rapidly: within 3 days of treatment (Lee and Bar-Sagi 2010). Here, the Ras oncogene was shown to suppress the senescence machinery. This offers a striking reversal of roles of oncogene activity and inflammation in regards to senescence. In the tumorigenic setting, there have been several demonstrations of recruitment of immune cells to the tumor site, in which these cells appear to induce the senescence of tumor cells.

In both cases the absence of senescent cells could be attributed to the inflammatory process preventing the ability of the epithelial cells to acquire the senescent phenotype to begin with; alternatively, inflammatory cells could act swiftly to remove senescent cells immediately upon their formation. Inflammation: Eliminating or Inducing Senescence? The relationship between senescent cells and the immune system cannot, however, be interpreted only in this antagonistic light. Several studies have revealed instances in which immune cells appear to promote cellular senescence.

Alternatively, cytokine secretion by senescent cells could negatively influence tissue function, and chronic low level inflammation induced by such cytokines could represent one means of ongoing damage to the tissue (Rodier and Campisi 2011). A recent study has provided an elegant demonstration of the negative effect exerted by senescent cells on their environment. Mice harboring a hypomorphic mutation in the mitotic checkpoint protein BubR1 suffer from premature aging phenotypes, including kyphosis, cachexia, cataracts, dermal thinning, as well as a shortened lifespan (Baker et al.

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